Contrast-induced Neurotoxicity Research Articles

Clinical management of contrast-induced neurotoxicity: a systematic review.

Contrast-induced neurotoxicity (CIN) is an increasingly recognised complication following endovascular procedures utilising contrast. It remains poorly understood with heterogenous clinical management strategies. The aim of this review was to identify commonly employed treatments for CIN to enhance clinical decision making. A systematic search of Embase (1947-2022) and Medline (1946-2022) was conducted. Articles describing (i) patients with a clinical diagnosis of CIN, (ii) with radiological exclusion of other pathologies, (iii) detailed report of treatments, and (iv) discharge outcomes, were included. Data relating to demographics, procedure, symptoms, treatment and outcomes were extracted. A total of 73 patients were included, with a median age of 64years. The most common procedures were cerebral angiography (42.5%) and coronary angiography (42.5%), and the median volume of contrast administered was 150ml. The most common symptoms were cortical blindness (38.4%) and reduced consciousness (28.8%), and 84.9% of patients experienced complete resolution at the time of discharge. Management included intravenous fluids to dilute contrast in the cerebrovasculature (54.8%), corticosteroids to reduce blood-brain barrier damage (47.9%), antiseizure (16.4%) and sedative (16.4%) medications. Mannitol (13.7%) was also utilised to reduce cerebral oedema. Intensive care admission was required for 19.2% of patients. No statistically significant differences were observed between treatment and discharge outcomes. The clinical management of CIN should be considered on a patient-by-patient basis, but may consist of aggressive fluid therapy alongside corticosteroids, as well as other supportive therapy as required. Further examination of CIN management is required to define best practice.

Development of vasogenic cerebral oedema after CT myelogram with nonionic contrast.

Madam, Cerebral edema is fluid accumulation in brain because of a cerebral injury such as trauma, ischemia, hemorrhage, abscess, tumors, and poisoning. Based on the pathophysiology it is divided into three types cytotoxic, interstitial and vasogenic, among which vasogenic edema is the commonest type.  [1] Vasogenic edema is a very rare complication of CT myelogram. A 42-year-old female known case of diabetes, hypertension, focal segmental necrotizing glomerulonephritis, and permanent pacemaker in situ for ASD secundum presented in December 2020 to Aga Khan University Hospital with backache and progressive bilateral lower limb weakness. On clinical examination she was conscious, alert, and oriented. She had a power of 4/5 and +2 reflexes in both the right and left upper limb and a power of 0/5 and absent reflexes in both the lower limbs. Patient was advised CSF studies and CT myelogram. CT myelogram was performed after a lumbar puncture at L3-L4 level. Approximately 12 mL of non-ionic water-soluble contrast was administered into the spinal canal. CT myelogram was normal. CSF studies showed raised protein. Within less than twelve hours she developed altered sensorium and decreased consciousness. Contrast-enhanced CT brain was performed which showed diffuse effacement of cortical sulci with poor gray-white matter differentiation as shown in Figure 1. There was crowding at the foramen magnum with evidence of tonsillar herniation as shown in Figure 2 and 3. Diagnosis of CT myelogram-induced cerebral edema was made. The patient received mannitol along with steroid pulse therapy. There was interval resolution of cerebral edema and tonsillar herniation on follow up CT brain (Figure 4 and 5). Endocrinology was taken onboard for the management of her diabetes. Five doses of pulse therapy were given, and after a five-day admission and observation the patient was discharged in stable condition. CT lumbar myelogram is a well-tolerated commonly performed procedure that employs intrathecal contrast to outline the subarachnoid space. The adverse effects of intrathecal contrast injection include nausea, headache, vomiting, and dizziness due to increase pressure in the subarachnoid spaces. Rare contrast-induced neurotoxicity, status epilepticus seizures and aseptic meningoencephalitis has also been reported with intrathecal and intravascular nonionic contrast agents. [3–5] Cerebral edema is also a rare complication of intrathecal contrast injection with few case reports being described in the literature. [2] We are reporting this case so that clinicians are familiar with this uncommon complication of CT myelogram to start early management for better patient outcome.

Current knowledge and perspectives of contrast-induced neurotoxicity: A survey of Australian clinicians

BackgroundContrast-induced Neurotoxicity (CIN) is an increasingly recognised complication following endovascular procedures. It remains a relatively unexplored clinical entity, and we sought to characterise clinician perspectives towards CIN, as well as identify gaps in knowledge and provide directions for future research. MethodsAn online survey was distributed to members of the Australian and New Zealand Society of Neuroradiology, as well as several Australian tertiary hospitals. Questions related to clinical exposure to CIN, diagnosis, management and pathophysiology were explored. Descriptive analysis was conducted on survey responses, and statistical analysis was performed using Chi-square and Fisher’s exact test as appropriate. ResultsA total of 95 survey responses were recorded (26.8% response rate). Only 28.4% of respondents were comfortable in diagnosing CIN, and even fewer (24.2%) were comfortable in independently managing CIN patients. Based on clinician opinion, symptoms including impaired consciousness and cortical blindness were thought to be most associated with CIN, whilst the radiological findings of parenchymal oedema and cortical enhancement were considered to be most indicative of CIN. Most clinicians agreed that further investigation is required related to pathophysiology (86.3%), diagnosis (83.2%), and treatment (82.1%). ConclusionCIN is a poorly understood complication following endovascular procedures. Significant gaps in clinical understanding are evident, and further investigation is vital to improve diagnosis and management.

Contrast-induced neurotoxicity presented as transient cortical blindness after stent-assisted coiling of a medium-sized unruptured basilar artery aneurysm: A case report and review of the literature

Background: Contrast-induced neurotoxicity is a rare event after endovascular diagnostic procedures or interventions and presents as transient neurological deficit. Herewith, we present a case of reversible complete cortical blindness after uneventful stent-assisted coiling of a medium-sized unruptured basilar artery aneurysm.Case Description: A 70-year-old woman with a medium-sized 10 mm/6 mm wide neck basilar tip aneurysm was planned for endovascular obliteration of the lesion. The procedure was done under general anesthesia. The contrast agent was iso-osmolar, nonionic. The aneurysm was coiled, and a stent was placed in the left posterior cerebral artery achieving sufficient aneurysm packing. No signs of vessel obliteration were observed during the procedure. On awakening of anesthesia, the patient reported complete visual loss. Ophthalmological examination was normal. The patient was brought back to the angio-suite but there were no signs of parent vessel compromise from the endovascular implants or distal vessel occlusion. An MRI of the brain was done showing no signs of brain ischemia, just mild brain edema in both occipital lobes. Given the results of the radiological studies and clinical presentation, the diagnosis of contrast-induced neurotoxicity was accepted. In 72 h, the patient had complete resolution of the visual loss and was discharged home with no additional neurological worsening.Conclusion: Contrast-induced neurotoxicity is a rare event that can occur after uneventful endovascular interventions of the brain vessels. Knowledge of this rare complication, after exclusion of all other possible reversible causes, is important for the treatment and prognosis of the patient.

Contrast-Induced Encephalopathy Post Cardiac Catheterization, A Rare Mimicry of Acute Stroke - Case Presentation and Review of the Literature.

Contrast-induced encephalopathy (CIE) or contrast-induced neurotoxicity is a rare, elusive, and puzzling diagnostic entity, even for most astute clinicians. Only a handful of publications have been written describing this rare phenomenon. A recent systematic review has only identified a total of 52 cases between 1970 - 2017 [1]. The most common neurological complication associated with cardiac catheterization is an atheroembolic stroke. CIE is not a well-known complication. Clinicians involved in administering high volumes of contrast solutions, as seen in coronary catheterizations, should be aware of this complication as it may be misdiagnosed as an acute stroke, leading to unnecessary additional contrast administration for imaging, as well as invasive and non-invasive interventions. In this report we present a case of an 87-year-old woman known coronary artery disease (CAD) who presented with acute coronary syndrome (ACS) and underwent a successful cardiac catheterization with stent placement followed by left-sided weakness a few hours later due to CIE. We also provide review of the literature and discuss management strategy of this rather rarely encountered diagnosis.

Greater intraprocedural systolic blood pressure and blood pressure variability are associated with contrast-induced neurotoxicity after neurointerventional procedures

BackgroundContrast-induced neurotoxicity (CIN) is a rare complication of neurointerventional procedures and its understanding remains limited. We evaluated the association of CIN with systemic hemodynamics in patients undergoing neuroendovascular interventions. MethodsWe conducted a 1:2 matched case-control study from a prospectively collected database of 2510 neurointerventional patients. We defined CIN as new neurological deficits presented ≤24 h post-operation after excluding other possible etiologies. We obtained demographic, clinical and imaging data, and baseline and intraprocedural blood pressures (BP) from medical records. The area between baseline and intraprocedural BP was used to measure sustained variability of BP over time. A generalized linear mixed model and generalized estimating equation were used to analyze the BP difference between groups over time. ResultsWe evaluated 11 CIN cases and 22 controls. 2746 and 5837 min of continued BP data were analyzed for cases and controls, respectively. CIN cases had higher measurements and greater variability for: Systolic BP (SBP) [median 125 (IQR:121–147) vs. 114 (IQR:107–124) mmHg], median area above baseline [median 350 (IQR:25–1328) vs. 52 (IQR:0–293) mmHg*minutes] and mean arterial pressure (MAP) [median 85 (IQR:79–98) vs. 80 (IQR:74–89) mmHg]. CIN cases demonstrated a significant mean increase in SBP and MAP of 23.41 mmHg (p < 0.01) and 13.79 mmHg (p < 0.01) when compared to controls, respectively, over the perioperative time. ConclusionSustained hypertension and high BP variability may contribute to the pathophysiology of CIN. Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms.

Contrast-induced neurotoxicity related to neurological endovascular procedures: a systematic review.

Contrast-induced neurotoxicity (CIN) is an adverse reaction to contrast agents which can occur in the context of diagnostic and therapeutic neurological endovascular procedures. Our goal was to conduct a systematic review of patients reported in the literature diagnosed with CIN after neurological endovascular procedures. A systematic search of EMBASE and MEDLINE databases was conducted. Inclusion criteria were age ≥ 18years; neurological endovascular procedure performed ≤ 24h before ictus; new manifestations compatible with encephalic dysfunction; imaging performed < 7days after ictus; exclusion of other causesand manifestations attributed to pre-existing conditions. Forty-eight patients were included, of which 60.4% were female and 60.4% had arterial hypertension; median age was 63years. The most frequent procedure was diagnostic cerebral angiography (n = 24, 50.0%) and non-ionic contrast agents were more frequently used (n = 40, 83.3%). Twenty-six patients (54.2%) developed clinical manifestations compatible with CIN during or immediately after the procedure, and the most frequent manifestations were encephalopathy, cortical blindness and motor deficit. The most frequent imaging findings were cortical contrast enhancement on CT (n = 23/42), and cortical sulci effacement (n = 18/48). Most patients presented complete clinical recovery (89.6%) at a median time of 3days. Among patients with neuroimaging changes who underwent follow-up, complete regression of the abnormalities was shown in 81.5% at a median time of 5days. CIN is a rare adverse reaction in the context of neurological endovascular procedures. Recognition of clinical manifestations and typical imaging abnormalities, while excluding other causes, is essential for diagnosis.

Clinical and Imaging Features of Contrast-Induced Neurotoxicity After Neurointerventional Surgery

Contrast-induced neurotoxicity (CIN) is an infrequent complication of endovascular procedures, and its understanding remains poor. We aimed to study and characterize the clinical and imaging features of a case series of CIN after neurointerventional surgery. We reviewed all neuroendovascular consecutive procedures from September 2014 to November 2018. CIN was defined as new onset of neurologic deficits that occurred postoperatively after excluding other conditions. All demographic, clinical, procedural, and radiologic data were retrospectively analyzed and collected. Eleven cases of CIN in 1587 patients were identified out of 2510 procedures. The median age was 76 years (interquartile range [IQR], 65-81). The most common comorbidity was hypertension (82%). Median procedure time was 100 minutes (IQR, 80-130.5 minutes). All patients showed wide variability in intraprocedural blood pressure (BP) recordings with fluctuations from the baseline BP. Systolic BP ranged from 83 mm Hg below the patient baseline to 80 mm Hg above baseline. The median symptom onset was 4 hours (IQR, 0.8-9.5 hours). The CIN signs and symptoms presented gradually, initially with encephalopathy and later with focal signs. All patients had an initial computed tomography scan, which showed ipsilateral cerebral edema in 82% of patients. Two had contrast enhancement. Complete resolution of CIN symptoms was obtained in a median time of 3 days (IQR, 2.5-3 days). CIN should be considered in the context of the progressive onset of neurologic deficits after neuroendovascular procedures. A distinct imaging pattern of ipsilateral hemisphere edema in the absence of ischemia is usually identified. Variability in procedural BP might be a predisposing factor.

TRANSIENT CORTICAL BLINDNESS DUE TO CONTRAST-INDUCED NEUROTOXICITY AFTER CARDIAC CATHETERIZATION

Cortical blindness is a rare complication of cardiac catheterization and may be due to contrast-induced neurotoxicity (CIN). Risk factors include high doses of contrast media and impaired renal function. A 45-year-old female with hypertension, chronic kidney disease and diabetes presented with

The diagnosis of contrast-induced neurotoxicity

The diagnosis of contrast-induced neurotoxicity

Contrast-induced neurotoxicity after coronary angiography

Contrast-induced neurotoxicity (CIN) is a very rare complication of coronary angiography. Clinical presentations include encephalopathy, seizures, cortical blindness, and focal neurological deficits. An inherent difficulty in understanding the natural history of the condition as well as its risk factors and prognosis is the rarity of its occurrence. To date, there are only case reports published on this complication. This was a retrospective analysis of 9 patients with CIN (8 men, 1 woman; mean age, 64.6 ± 7.8 years; range, 47-72 years) and coronary artery disease who were administered iopromide contrast agent. In the last 3 years, we diagnosed 9 patients with CIN. Of these, 8 patients (89 %) had hypertension. The clinical presentations of the patients were different on admission: 6 patients had acute coronary syndrome and 3 patients had stable angina pectoris. One patient had history of previous contrast agent exposure. All patients underwent coronary angiography with a low-osmolar nonionic monomer contrast agent (iopromide; Ultravist®-300, Bayer Healthcare). The mean volume of contrast injected was 177 ± 58 ml. The mean time between contrast agent administration and clinical symptoms was 100 ± 71 min (range, 30-240 min). While in 5 of the patients (56 %) the clinical sign of CIN was confusion, 2 had ophthalmoplegia, 1 had cerebellar dysfunction, and 1 had monoplegia. In 8 of 9 patients (89 %), neurological symptoms resolved after giving supportive medication and hydration. Only 1 female patient, who had bilateral ophthalmoplegia, did not recover. Neurological recovery occurred at a mean time of 14.2 ± 6.7 h (range, 8-30 h). CIN is a very rare condition. Advanced age, male gender, and hypertension are the greatest risk factors for CIN. Although the prognosis of CIN is benign, it can potentially cause permanent neurological deficits or death. We found that patients with ophthalmic involvement had a higher propensity for persistent deficit. On the basis of the current data, we propose 170 ml as the maximal recommended dose for coronary procedures.

Contrast-Induced Neurotoxicity following Cardiac Catheterization

We report a case of probable contrast-induced neurotoxicity that followed a technically challenging cardiac catheterization in a 69-year-old woman. The procedure had involved the administration of a large cumulative dose of an iodinated, nonionic contrast medium into the innominate artery: twelve hours following the catheterization, the patient developed a seizure followed by a left hemiplegia, and an initial computed tomography (CT) scan showed sulcal effacement in the right cerebral hemisphere due to cerebral swelling. The patient's clinical symptoms resolved within 24 hours, and magnetic resonance imaging at 32 hours showed resolution of swelling. Contrast-induced neurotoxicity should be found in the differential diagnosis of acute neurological deficits occurring after radiological procedures involving iodinated contrast media, whether ionic or nonionic.

Aseptic Meningoencephalitis after Iohexol CT Myelography

We describe the case of a patient with aseptic meningoencephalitis after intrathecal iohexol injection for myelography and review the previous literature on similar cases of contrast-induced neurotoxicity.